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Androgen is the generic term for any natural or synthetic compound, usually a steroid hormone, that stimulates or controls the development and maintenance of masculine characteristics in vertebrates by binding to androgen receptors. This includes the activity of the accessory male sex organs and development of male secondary sex characteristics. Androgens, which were first discovered in 1936, are also called androgenic hormones or testoids. Androgens are also the original anabolic steroids. They are also the precursor of all estrogens, the female sex hormones. The primary and most well-known androgen is testosterone. Androgen ablation can be used as an effective therapy in prostate cancer.

Contents

Types

Steroidogenesis, showing the relation between several androgens at bottom left. (Estrone and estradiol, in contrast, are estrogens.

A subset of androgens, adrenal androgens, includes any of the 19-carbon steroids synthesized by the adrenal cortex, the outer portion of the adrenal gland (zonula reticularis—innermost region of the adrenal cortex), that function as weak steroids or steroid precursors, including dehydroepiandrosterone (DHEA), dehydroepiandrosterone sulfate (DHEA-S), and androstenedione.

Besides testosterone, other androgens include:

  • Androsterone: a chemical by-product created during the breakdown of androgens, or derived from progesterone, that also exerts minor masculinising effects, but with one-seventh the intensity of testosterone. It is found in approximately equal amounts in the plasma and urine of both males and females.

Androgen functions

Development of the male

Testes formation

During mammalian development, the gonads are at first capable of becoming either ovaries or testes.[1] In humans, starting at about week 4 the gonadal rudiments are present within the intermediate mesoderm adjacent to the developing kidneys. At about week 6, epithelial sex cords develop within the forming testes and incorporate the germ cells as they migrate into the gonads. In males, certain Y chromosome genes, particularly SRY, control development of the male phenotype, including conversion of the early bipotential gonad into testes. In males, the sex cords fully invade the developing gonads.

Androgen production

The mesoderm-derived epithelial cells of the sex cords in developing testes become the Sertoli cells which will function to support sperm cell formation. A minor population of non-epithelial cells appear between the tubules by week 8 of human fetal development. These are Leydig cells. Soon after they differentiate, Leydig cells begin to produce androgens.

Androgen effects

The androgens function as paracrine hormones required by the Sertoli cells in order to support sperm production. They are also required for masculinization of the developing male fetus (including penis and scrotum formation). Under the influence of androgens, remnants of the mesonephron, the Wolffian ducts, develop into the epididymis, vas deferens and seminal vesicles. This action of androgens is supported by a hormone from Sertoli cells,MIH (Mullerian Inhibitory Hormone), which prevents the embryonic Müllerian ducts from developing into fallopian tubes and other female reproductive tract tissues in male embryos. MIH and androgens cooperate to allow for the normal movement of testes into the scrotum.

Early regulation

Before the production of the pituitary hormone LH by the embryo starting at about weeks 11–12, human chorionic gonadotrophin (hCG) promotes the differentiation of Leydig cells and their production of androgens. Androgen action in target tissues often involves conversion of testosterone to 5α-dihydrotestosterone (DHT).

Spermatogenesis

During puberty, androgen, LH and FSH production increase and the sex cords hollow out, forming the seminiferous tubules, and the germ cells start to differentiate into sperm. Throughout adulthood, androgens and FSH cooperatively act on Sertoli cells in the testes to support sperm production.[2] Exogenous androgen supplements can be used as a male contraceptive. Elevated androgen levels caused by use of androgen supplements can inhibit production of LH and block production of endogenous androgens by Leydig cells. Without the locally high levels of androgens in testes due to androgen production by Leydig cells, the seminiferous tubules can degenerate resulting in infertility. For this reason, many transdermal androgen patches are applied to the scrotum.

Inhibition of fat deposition

Males typically have less adipose tissue than females. Recent results indicate that androgens inhibit the ability of some fat cells to store lipids by blocking a signal transduction pathway that normally supports adipocyte function.[3] Also, androgens, but not estrogens, increase beta adrenergic receptors while decreasing alpha adrenargic receptors- which results in increased levels of epinephrine/ norepinephrine due to lack of alpha-2 receptor negative feedback and decreased fat accumulation due to epinephrine/ norepinephrine then acting on lipolysis-inducing beta receptors.

Muscle mass

Males typically have more skeletal muscle mass than females. Androgens promote the enlargement of skeletal muscle cells and probably act in a coordinated manner to function by acting on several cell types in skeletal muscle tissue.[4] One type of cell that conveys hormone signals to generating muscle is the myoblast. Higher androgen levels lead to increased expression of androgen receptor. Fusion of myoblasts generates myotubes, in a process that is linked to androgen receptor levels.[5]

Brain

Circulating levels of androgens can influence human behavior because some neurons are sensitive to steroid hormones. Androgen levels have been implicated in the regulation of human aggression[6] and libido. Indeed, androgens are capable of altering the structure of the brain in several species, including mice, rats, and primates, producing sex differences.[7] Although, their potential for conversion makes identifying which alterations in neuroanatomy stem from androgens or estrogens slightly difficult, numerous reports have outlined that androgens alone are capable of altering the structure of the brain.[8]

Insensitivity to androgen in humans

Reduced ability of a XY karyotype fetus to respond to androgens can result in one of several conditions, including infertility and several forms of intersex conditions.

See also

References

  1. ^ Scott F. Gilbert; with a chapter on plant development by Susan R. Singer (2000). Scott F. Gilbert. ed. Developmental Biology (6th ed.). Sunderland, Massachusetts: Sinauer Associates. ISBN 0-87893-243-7. http://www.ncbi.nlm.nih.gov/books/bv.fcgi?rid=dbio.  
  2. ^ Stephen Nussey and Saffron Whitehead (2001). Saffron A. Whitehead and Stephen Nussey. ed. Endocrinology: an integrated approach. Oxford: British Institute of Organ Studies. ISBN 1-85996-252-1. http://www.ncbi.nlm.nih.gov/bookshelf/br.fcgi?book=endocrin.  
  3. ^ Singh R, Artaza JN, Taylor WE, et al. (January 2006). "Testosterone inhibits adipogenic differentiation in 3T3-L1 cells: nuclear translocation of androgen receptor complex with beta-catenin and T-cell factor 4 may bypass canonical Wnt signaling to down-regulate adipogenic transcription factors". Endocrinology 147 (1): 141–54. doi:10.1210/en.2004-1649. PMID 16210377.  
  4. ^ Sinha-Hikim I, Taylor WE, Gonzalez-Cadavid NF, Zheng W, Bhasin S (October 2004). "Androgen receptor in human skeletal muscle and cultured muscle satellite cells: up-regulation by androgen treatment". The Journal of Clinical Endocrinology and Metabolism 89 (10): 5245–55. doi:10.1210/jc.2004-0084. PMID 15472231.  
  5. ^ Vlahopoulos S, Zimmer WE, Jenster G, et al. (March 2005). "Recruitment of the androgen receptor via serum response factor facilitates expression of a myogenic gene". The Journal of Biological Chemistry 280 (9): 7786–92. doi:10.1074/jbc.M413992200. PMID 15623502.  
  6. ^ Singh R, Artaza JN, Taylor WE, et al. (January 2006). "Testosterone inhibits adipogenic differentiation in 3T3-L1 cells: nuclear translocation of androgen receptor complex with beta-catenin and T-cell factor 4 may bypass canonical Wnt signaling to down-regulate adipogenic transcription factors". Endocrinology 147 (1): 141–54. doi:10.1210/en.2004-1649. PMID 16210377.  
  7. ^ Cooke B, Hegstrom CD, Villeneuve LS, Breedlove SM (October 1998). "Sexual differentiation of the vertebrate brain: principles and mechanisms". Frontiers in Neuroendocrinology 19 (4): 323–62. doi:10.1006/frne.1998.0171. PMID 9799588.  
  8. ^ Zuloaga DG, Puts DA, Jordan CL, Breedlove SM (May 2008). "The role of androgen receptors in the masculinization of brain and behavior: what we've learned from the testicular feminization mutation". Hormones and Behavior 53 (5): 613–26. doi:10.1016/j.yhbeh.2008.01.013. PMID 18374335.  







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